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Nonarteritic anterior ischemic optic neuropathy:

cause, effect, and management

This article was published in the following Dove Press journal:

Eye and Brain
27 September 2017
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Shauna Berry 1 Abstract: Nonarteritic anterior ischemic optic neuropathy (NAION) is the most common form of
Weijie V Lin 2 ischemic optic neuropathy and the second most common optic neuropathy. Patients are generally
Ama Sadaka 1 over the age of 50 years with vasculopathic risk factors (eg, diabetes mellitus, hypertension, and
Andrew G Lee 1–7 obstructive sleep apnea). The exact mechanism of NAION is not fully understood. In addition,
several treatment options have been proposed. This article summarizes the current literature on
1
Department of Ophthalmology,
Blanton Eye Institute, Houston the diagnosis, treatment, and management of NAION.
Methodist Hospital, Houston, TX, Keywords: anterior ischemic optic neuropathy, nonarteritic anterior ischemic optic neuropathy,
USA; 2Department of Ophthalmology, ischemic optic neuropathy
Baylor College of Medicine,
Houston, TX, USA; 3Department of
Ophthalmology and Visual Sciences,
University of Texas Medical Branch
Introduction
(UTMB), Galveston, TX, USA; Nonarteritic anterior ischemic optic neuropathy (NAION) is the second most common
4
Department of Ophthalmology,
5
Department of Neurology,
optic neuropathy after glaucoma caused by infarction of the short posterior ciliary
6
Department of Neurosurgery, Weill arteries that supply the anterior portion of the optic nerve head. This leads to axonal
Cornell Medicine, Houston, TX, USA;
edema and a compartment syndrome in an already crowded optic disc causing vision
7
Department of Ophthalmology, The
University of Texas MD Anderson loss.1 Annually, there are ~6,000 new cases in the United States.1 Significant research on
Cancer Center, Houston, TX, USA pathophysiology, prevention, and treatment has been performed and will be discussed
in this review, but remains limited.

Clinical presentation and pathogenesis

NAION typically presents with acute unilateral painless vision loss accompanied by
sector or diffuse optic nerve edema.2 It occurs more frequently in the Caucasian popu-
lation and there is no gender predilection.1,2 It generally affects people over 50 years
of age, with a mean onset between 57 and 65 years of age. However, it has also been
reported in patients <40 years old both with and without vasculopathic risk factors (ie,
NAION of the young [NAIONY]).3 Visual field (VF) defects following a nerve fiber
layer distribution are typical VF findings, with inferior altitudinal and arcuate defects
being the most common.1,2,4 Patients may describe the vision loss as a “dim or blur”,
especially in the area of the field loss.1 Hayreh et al noted that vision loss was often
Correspondence: Andrew G Lee reported upon awakening, and some authors believe that the etiology for NAION is
Department of Ophthalmology, Blanton nocturnal hypotension.5 Vision loss from NAION is variable but is typically less severe
Eye Institute, Houston Methodist
Hospital, 6560 Fannin Street, Suite 450, than the loss from arteritic anterior ischemic optic neuropathy (A-AION). Hayreh et al
Houston, TX 77030, USA observed the initial visual acuity (VA) to be 20/30 or better in 49% of cases of NAION.5
Tel +1 713 441 8843
Fax +1 713 793 1636 An ipsilateral relative afferent pupillary defect will be present in unilateral or bilateral
Email aglee@houstonmethodist.org but asymmetric cases. Sector or diffuse disc edema in the acute phase of the disease is

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essential for clinical diagnosis. The disc edema may or may meningioma, and infectious, infiltrative, or inflammatory
not be accompanied by peripapillary hemorrhages.3 Macular optic neuropathies). There is up to a 15% chance of fellow eye
edema and exudates are less common. involvement at 5 years.14,15 The VA and VF defect in a patient
Although the exact pathogenesis of NAION remains with prior NAION cannot directly predict the prognosis of
unproven, it appears to be a multifactorial disease.4 It is visual impairment if there is second eye involvement.12,13
presumed to be due to a transient disruption in the circula- This presentation of optic disc edema in one eye and optic
tion of the optic nerve head leading to hypoperfusion and atrophy in the fellow eye can produce a “pseudo-Foster
ischemia. The exact cause of this transient disturbance Kennedy” syndrome. The key in differentiating between
remains unclear but several hypotheses have been proposed “pseudo-Foster Kennedy” and a true Foster Kennedy is the
including generalized hypoperfusion, nocturnal hypotension, history of abrupt vision loss in the affected eye with optic
local autoregulation failure, vasospasm, venous occlusion, disc edema (acute NAION) and a history of prior visual loss
and thrombosis. In addition, patients with NAION typically in the contralateral eye with optic atrophy (old NAION). In
have a small cup-to-disc ratio as a predisposing factor, and the true Foster Kennedy syndrome, there is no abrupt vision
this “crowded optic disc head” has been referred to as the loss as the pale disc is from a compressive etiology and the
“structural disc at risk” for NAION. Theoretically, when fellow edematous disc is secondary to papilledema from
localized swelling occurs in a fixed space anterior to the rigid increased intracranial pressure.1
lamina cribosa, the capillaries could become more easily
compressed and secondary ischemia may result.1,2 Recent Management and treatment
studies of the optic nerve head utilizing optical coherence NAION is primarily a clinical diagnosis. The most important
tomography (OCT) have demonstrated thicker prelaminar initial step in management is to exclude giant cell arteritis
tissue in NAION patients.7 Systemic diseases that may (ie, A-AION). The presence of pallid edema on exam and
cause decreased perfusion to the optic nerve head secondary symptoms including pain, jaw claudication, scalp tenderness,
to microvascular compromise might increase the patient’s fever, and malaise should raise suspicion for A-AION.
risk of NAION. These include hypertension, diabetes, and Patients presenting with typical features generally do not
hypercholesterolemia. Other risk factors noted in the litera- need neuroimaging or additional laboratory testing other than
ture are nocturnal hypotension, smoking, obstructive sleep erythrocyte sedimentation rate (ESR), C-reactive protein
apnea, anemia, hypercoagulable states, disc drusen, ocular (CRP), or platelet count.16 Other causes of optic neuropathies
and nonocular surgery, and migraines. The use of vasoactive should be considered in the presence of atypical features.
medications may be an additional risk factor for NAION. Table 1 summarizes some of the atypical features. Some
Phosphodiesterase type-5 inhibitors (PDE-5i) have recently patients may require cranial and orbital magnetic resonance
been implicated in NAION; however, there is still much imaging (MRI; eg, progressive NAION) and, rarely, head
debate over this topic. A recent observational study reported and neck MR-angiogram (MRA) or computed tomography
an increase of 2.21 in the odds ratio of an NAION in patients angiography (CTA) may be considered in patients present-
using PDE-5i up to 30 days prior2,8 to the event. Amiodarone ing with unilateral head or neck pain to exclude a carotid
has also been associated with NAION.9 dissection.1–3,17,18

Table 1 Atypical features for NAION

Prognosis
Although a progressive form of NAION has been reported, Less than 40 years old
Pain
the course of NAION typically stabilizes within 2–3 months.1 Bilateral simultaneous onset
The visual prognosis is generally guarded; however, the acuity Rapidly sequential vision loss
may improve by up to three lines in 43% of patients.1,10 The Lack of optic disc edema
VF defects are less likely to improve. There is <5% chance Optic disc edema persisting >4 weeks
Atypical VF defect (homonymous hemianopia)
of recurrence in the same eye.1,11 The initial disc edema usu- Absence of a relative afferent pupillary defect
ally resolves, and sector or diffuse atrophy ensues typically Lack of vasculopathic risk factors
within the next 6–11 weeks.1 Large cup-to-disc ratio in the fellow eye
Recurrent attacks
Work-up for other etiologies of optic disc edema, how-
Macular star
ever, should be considered if the edema persists beyond
Abbreviations: VF, visual field; NAION, nonarteritic anterior ischemic optic
this time frame (eg, compressive lesion, optic nerve sheath neuropathy.

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Dovepress Cause, effect, and management of NAION

A thorough history, including medications (eg, PDE-5i, To date, no definitive high-grade evidence for an effec-
amiodarone), past medical history (eg, vasculopathic risk tive treatment of NAION exists (Table 2). The highest level
factors), recent surgical history, and social history (eg, smok- of evidence comes from the Ischemic Optic Neuropathy
ing), is key. Patients should be evaluated by their primary Decompression Trial (IONDT).1,2,10 This was a prospective,
care physicians for modifiable risk factors including hyper- randomized trial that assessed optic nerve sheath fenestration
tension, hyperlipidemia, diabetes mellitus, and obstructive as a treatment for NAION. It was the only randomized con-
sleep apnea. trolled trial for NAION. It was based upon the theory that an
A carotid workup is generally not indicated in typical optic nerve sheath fenestration could reduce the compartment
NAION but can be considered in the presence of ocular syndrome effect.1 However, the study concluded that optic
ischemic syndrome, retinal emboli, or transient neurological nerve sheath fenestration was not an effective intervention
deficits.19 OCT can be used to monitor the disease course for and may actually have a harmful effect.10
long term with the assessment of edema and optic atrophy, Other treatment options explored include medical thera-
but NAION remains a clinical diagnosis and there are no pies such as aspirin, steroids, and neuroprotective agents.
diagnostic OCT features of NAION. Some recent stud- Aspirin has been studied as a primary treatment for NAION
ies have demonstrated the use of OCT in the assessment, as well as a preventive measure of fellow eye involvement. A
diagnosis, and management of NAION.6, 20 Findings include retrospective case-controlled study showed no improvement in
increased peripapillary choroidal thickness associated with the final visual outcome in those treated with aspirin before,
optic disc edema and subretinal fluid on spectral domain during, and following NAION compared with those who did
OCT (SD-OCT) and macular ganglion cell inner plexiform not receive any aspirin.27 The majority of the retrospective and
layer thinning associated with VF defect in frequency case-control studies examined aspirin for its use in preventing
domain OCT (FD-OCT). 6, 21 Another study found that NAION in the fellow eye.12,14,27,28 Data from the retrospective
NAION affected neither the cup-to-disc ratio nor alpha or studies are controversial. The most convincing data come from
beta zone of parapapillary atrophy.22 Ganglion cell layer plus the follow-up to the Ischemic Optic Neuropathy Decompres-
inner plexiform layer (GCL+IPL) thinning has been shown sion Trial (IONDT) and a large retrospective review by Beck
to be better than retinal nerve fiber layer (RNFL) thinning in et al. The IONDT follow-up suggested that aspirin did not
indicating early structural loss in NAION.23 The application influence the rate of recurrence.15 The large retrospective study
of OCT-angiography (OCT-A) in NAION is also being stud- of 431 patients with NAION by Beck et al suggests a possible
ied. OCT-A is a useful noninvasive technique in depicting short-term benefit of aspirin (cumulative probability of 7% in
ocular perfusion in comparison to fluorescein angiography. aspirin group and 15% in non-aspirin group at 2 years) but
It can also be used in pregnant patients and those allergic to lacks a long-term benefit in reducing the risk of NAION in
fluorescein. A case study by Higashiyama et al demonstrated the fellow eye (17% aspirin group vs 20% untreated group
areas of decreased retinal perfusion on OCT-A consistent at 5 years).14 Despite sufficient evidence of long-term ben-
with the RNFL and gangion cell complex loss in NAION.24 efit of aspirin, many still recommend it following the initial
Another study by Sharma et al examined the microvascular NAION because of the vasculopathic risk factors associated
perfusion during the acute and follow-up stages of NAION. with NAION. This becomes more important when consider-
OCT-A demonstrated segmental and global reduction of ing the data on increased risk of ischemic stroke in patients
the peripapillary flow in the acute phase with subsequent with NAION. A recent retrospective study found a 3.35 times
spontaneous partial recovery consistent with visual recovery increased risk of developing an ischemic stroke in patients
and the natural course of NAION. Furthermore, the temporal with NAION compared to patients with similar comorbidities
sector of the nerve head not only demonstrated the highest but without NAION.29 However, like much of the data, there
flow density in healthy controls, but also demonstrated is conflicting opinions in this association.29, 30
the most damage in eyes with NAION.25 They also found Steroids, administered systemically, periocularly, or intra-
that there was no disruption of the microvasculature in the ocularly, have been proposed as treatment modalities with the
healthy unaffected eye. The authors proposed that this could earliest report dating back to the late 1960s.1–3, 31, 32 The initial
be subsequent to the temporal watershed zone discussed by study demonstrated improvement in 11 of 13 (85%) patients
Hayreh26 which correlates with the predominance of nasal treated with 60 mg/day oral prednisone compared to 5 of 11
field defects in NAION. (45%) untreated patients. The authors postulated that steroids

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Berry et al Dovepress

Table 2 Summary of some of the studies that explored treatment of NAION

Treatment Hypothesized Type of study (level of Outcome
mechanism of action evidence)
Surgical
ONSD To resolve the Masked, prospective, 32.6% surgery patients improved compared to 42.7% of
“compartment syndrome” randomized (I) observation group12,20
RON To resolve the Randomized, control (II) 75% of eight treated eyes improved with RON, one eye
“compartment syndrome” developed a choroidal neovascular membrane. 25% of eight
untreated eyes improved18
Systemic
Systemic corticosteroids Decreased disc swelling Nonrandomized VA improved in 69.8% of 236 treated patients and in 40.5%
controlled study (III) of 301 untreated. VF improved in 40.1% of treated patients
and in 24.5% of untreated3
Combined systemic Decrease disc swelling Prospective No benefit in combined corticosteroids and erythropoietin
corticosteroids and and neuroprotection interventional case series versus systemic corticosteroids alone versus control in
erythropoietin final VA
Oral levodopa Neuroprotection Retrospective, 76.9% of 18 treated improved
nonrandomized 30% of 19 untreated improved
Aspirin Improves blood flow Retrospectivea IONDT showed no association between regular aspirin use
and the incidence of fellow eye NAION12,20
Topical
Topical brimonidine Neuroprotection Multicenter, randomized, No VF or VA improvements. Both trials NPION and
clinical trial (II) BRAION discontinued due to recruitment difficulties
Retrospective (III) Treated patients had worse outcomes in all visual
parameters14
Intravitreal
Intravitreal steroids Decreased disc edema Case controlled (III) VA improved in 4 treated and 6 untreated18
Intravitreal erythropoietin Neuroprotection Prospective case series 61.2% VA improved with treatment, but no VF
improvement19
Intravitreal anti-VEGF Reduced vasogenic disc Various case reports, A faster resolution of disc edema and improved visual
swelling case series (IV) outcome were documented15
Intravitreal injection of QPI- Neuroprotection Clinical trial is still
1007 (siRNA) recruiting patients
Note: aThe IONDT was a prospective trial to evaluate ONSD in the management of NAION. Aspirin data were observational only.
Abbreviations: IONDT, Ischemic Optic Neuropathy Decompression Trial; NAION, nonarteritic anterior ischemic optic neuropathy; ONSD, optic nerve sheath
decompression; RON, radial optic neurotomy; siRNA, small interfering ribonucleic acid; VA, visual acuity; VEGF, vascular endothelial growth factor; VF, visual field.

would decrease the capillary permeability, subsequently oxygen, and transcorneal electrical stimulation have been
accelerating the resolution of the disc edema and reducing explored.36–45 However, these studies are limited by their
the compressions of capillaries on the optic nerve head and small number of patients and absence of control. Emerging
therefore improving blood flow to ischemic axons.31,33 Hayreh on the forefront of neuroprotective efforts is intravitreal
and Zimmerman conducted a large nonrandomized study in small interfering ribonucleic acid (siRNA) injections. siRNA
which patients could elect to be treated with oral prednisone prevents apoptosis by inhibiting the expression of caspase-2.
80 mg/day for 14 days followed by a 2-month taper. The This randomized, double-masked study is still in the patient
authors observed improvement of visual function in those recruitment phase with no data available yet.46
treated compared to the untreated controls. However, the
nonrandomized and unmasked nature of the study, the older Conclusion
age and higher vasculopathic comorbidities of their untreated NAION remains a common disease with devastating conse-
patients, and the large steroid dose that carries systemic side quences for patients, unclear pathophysiology, and contradic-
effects with it weaken the findings.34 Evidence for intravitreal tory data regarding fellow eye involvement and treatment.
administration of steroids remains controversial.35 In our experience, if you are considering the diagnosis
Additional treatment efforts aimed at neuroprotection of NAION in a patient presenting with acute vision loss and
with agents such as intravitreal erythropoietin, oral levodopa, optic disc edema, we recommend that you think of the fol-
diphenylhydantoin, topical brimonidine tartrate, hyperbaric lowing: 1) look for atypical features that would make you

26 submit your manuscript | www.dovepress.com Eye and Brain 2017:9

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Dovepress Cause, effect, and management of NAION

consider diagnoses other than NAION (Table 1); 2) ask about 14. Beck RW, Hayreh SS, Podhajsky PA, Tan ES, Moke PS. Aspirin therapy
in nonarteritic anterior ischemic optic neuropathy. Am J Ophthalmol.
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problems that can be associated with the disc edema such as 15. Newman NJ, Scherer R, Langenberg P, et al. The fellow eye in NAION:
inflammatory and neoplastic diseases; 3) if the patient is in report from the ischemic optic neuropathy decompression trial follow-up
study. Am J Ophthalmol. 2002;134(3):317–328.
the appropriate age group, has vasculopathic risk factors, has 16. Arnold AC, Hepler RS, Hamilton DR, Lufkin RB. Magnetic resonance
a disc at risk in the fellow eye, and has no atypical features, imaging of the brain in nonarteritic ischemic optic neuropathy. J Neur-
oophthalmol. 1995;15(3):158–160.
then you can make a diagnoses of NAION, but continue to 17. Biousse V, Schaison M, Touboul PJ, D’Anglejan-Chatillon J, Bousser
monitor the patient. Once the diagnoses of NAION is made, MG. Ischemic optic neuropathy associated with internal carotid artery
we recommend counseling the patient about better control dissection. Arch Neurol. 1998;55(5):715–719.
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contraindication, to all our patients despite the lack of level 20. Balogh Z, Kasza M, Vardai J, et al. Analysis of optic disc damage by opti-
I evidence to prove benefit. The future holds promise with cal coherence tomography in terms of therapy in non-arteritic anterior
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tal non-arteritic anterior ischemic optic neuropathy. Eye (Lond).
Disclosure 2014;28(12):1494–1501.
22. Jonas JB, Hayreh SS, Tao Y, Papastathopoulos KI, Rensch F. Optic nerve
The authors report no conflicts of interest in this work. head change in non-arteritic anterior ischemic optic neuropathy and its
influence on visual outcome. PLoS One. 2012;7(5):e37499.
23. Kupersmith MJ, Garvin MK, Wang JK, Durbin M, Kardon R. Retinal
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